Evidence map›Paper›PMID 28714013›Full record

ArticleOncology reports2017

Glioblastoma entities express subtle differences in molecular composition and response to treatment.

Joana Balça-Silva, Diana Matias, Anália Do Carmo, Luiz Gustavo Dubois, Ana Cristina Gonçalves, Henrique Girão, Nathalie Henriques Silva Canedo, Ana Helena Correia, Jorge Marcondes De Souza, Ana Bela Sarmento-Ribeiro and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 2 countries.

Joana Balça-SilvaCenter for Neuroscience and Cell Biology and Institute for Biomedical Imaging and Life Sciences (CNC.IBILI), Coimbra, Portugal.
Diana MatiasInstituto Estadual do Cérebro Paulo Niemeyer (IECPN), Secretaria de Estado de Saúde, Rio de Janeiro, Brazil.
Anália Do CarmoCenter for Neuroscience and Cell Biology and Institute for Biomedical Imaging and Life Sciences (CNC.IBILI), Coimbra, Portugal.
Luiz Gustavo DuboisInstituto Estadual do Cérebro Paulo Niemeyer (IECPN), Secretaria de Estado de Saúde, Rio de Janeiro, Brazil.
Ana Cristina GonçalvesCenter for Neuroscience and Cell Biology and Institute for Biomedical Imaging and Life Sciences (CNC.IBILI), Coimbra, Portugal.
Henrique GirãoCenter for Neuroscience and Cell Biology and Institute for Biomedical Imaging and Life Sciences (CNC.IBILI), Coimbra, Portugal.
Nathalie Henriques Silva CanedoDepartment of Pathology, Clementino Fraga Filho Hospital, Federal University of Rio de Janeiro, School of Medicine, Rio de Janeiro, Brazil.
Ana Helena CorreiaDepartment of Pathology, Clementino Fraga Filho Hospital, Federal University of Rio de Janeiro, School of Medicine, Rio de Janeiro, Brazil.
Jorge Marcondes De SouzaDepartment of Neurosurgery, Clementino Fraga Filho Hospital, Federal University of Rio de Janeiro, School of Medicine, Rio de Janeiro, Brazil.
Ana Bela Sarmento-RibeiroCenter for Neuroscience and Cell Biology and Institute for Biomedical Imaging and Life Sciences (CNC.IBILI), Coimbra, Portugal.
Maria Celeste LopesCenter for Neuroscience and Cell Biology and Institute for Biomedical Imaging and Life Sciences (CNC.IBILI), Coimbra, Portugal.
Vivaldo Moura-NetoInstituto Estadual do Cérebro Paulo Niemeyer (IECPN), Secretaria de Estado de Saúde, Rio de Janeiro, Brazil.
Centro de Neurociências e Biologia CelularInstituto Estadual do Cérebro Paulo Niemeyer · BRAssociation for Innovation and Biomedical Research on Light and Image · PTHospital Universitário Clementino Fraga Filho · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is a grade IV astrocytoma. GBM patients show resistance to chemotherapy such as temozolomide (TMZ), the gold standard treatment. In order to simulate the molecular mechanisms behind the different chemotherapeutic responses in GBM patients we compared the cellular heterogeneity and chemotherapeutic resistance mechanisms in different GBM cell lines. We isolated and characterized a human GBM cell line obtained from a GBM patient, named GBM11. We studied the GBM11 behaviour when treated with Tamoxifen (TMX) that, among other functions, is a protein kinase C (PKC) inhibitor, alone and in combination with TMZ in comparison with the responses of U87 and U118 human GBM cell lines. We evaluated the cell death, cell cycle arrest and cell proliferation, mainly through PKC expression, by flow cytometry and western blot analysis and, ultimately, cell migration capability and f-actin filament disorganization by fluorescence microscopy. We demonstrated that the constitutive activation of p-PKC seems to be one of the main metabolic implicated on GBM malignancy. Despite of its higher resistance, possibly due to the overexpression of P-glycoprotein and stem-like cell markers, GBM11 cells presented a subtle different chemotherapeutic response compared to U87 and U118 cells. The GBM11, U87, U118 cell lines show subtle molecular differences, which clearly indicate the characterization of GBM heterogeneity, one of the main reasons for tumor resistance. The adding of cellular heterogeneity in molecular behaviour constitutes a step closer in the understanding of resistant molecular mechanisms in GBM, and can circumvents the eventual impaired therapy.

Indexed as

Genetic HeterogeneityApoptosisAstrocytomaATP Binding Cassette Transporter, Subfamily B, Member 1Cell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDacarbazineDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGlioblastomaHumansNeoplasm GradingProtein Kinase CSignal TransductionATP Binding Cassette Transporter, Subfamily B, Member 1DacarbazineProtein Kinase CTamoxifenTemozolomide

Identifiers

PMID28714013
PMCPMC5549060
OpenAlexW2725765951

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.